论文部分内容阅读
为考察野生型ｐ５３基因转移入舌鳞癌细胞株Ｔｃａ８１１３后，癌株在裸鼠体内的生长及增殖状态，作者采用电穿孔方法分４组进行了如下基因转移：野生型ｐ５３基因，空白对照质粒，突变型ｐ５３基因和未转移任何基因的空白对照。在基因转移进入舌鳞癌细胞株Ｔｃａ８１１３后，分别接种于１６只裸鼠体内。成瘤后分别进行常规病理学、定量病理学和免疫组织化学研究。结果：转染野生型ｐ５３基因组与其余３组比较，其形成的肿瘤重量明显为轻；肿瘤异常核分裂相减少；定量病理学显示肿瘤坏死区面积所占瘤体总面积的百分比明显降低；免疫组织化学显示非坏死区增殖细胞核抗原明显更低。上述结果提示肿瘤细胞获取了功能完好的外源性野生型ｐ５３基因后，其基因表达并产生了新的负性调节因子，抑制了肿瘤的生长和增殖。并从理论上证明了利用野生型ｐ５３基因口腔粘膜鳞癌进行基因治疗是可能的。
In order to investigate the growth and proliferation of cancer cells in nude mice after wild-type p53 gene transfer into tongue squamous cell carcinoma cell line Tca8113, the authors used electroporation to divide the following gene into four groups: wild-type p53 gene, blank control plasmid , mutant p53 gene and blank control without transfer of any gene. After gene transfer into tongue squamous carcinoma cell line Tca8113, they were inoculated into 16 nude mice. After tumor formation, routine pathology, quantitative pathology and immunohistochemistry were performed. RESULTS: Compared with the other three groups, the weight of the tumor cells transfected with wild-type p53 gene was significantly lighter, and the abnormal mitotic phase was decreased. Quantitative pathology showed that the percentage of tumor necrosis area accounted for a significant reduction in the percentage of total tumor area; The chemical shows that the proliferating cell nuclear antigen in the non-necrotic area is significantly lower. The above results suggest that the tumor cells obtain a fully functional exogenous wild-type p53 gene, and the gene expression of the exogenous wild-type p53 gene results in a new negative regulatory factor, which inhibits the growth and proliferation of the tumor. And theoretically proved that the use of wild-type p53 gene oral squamous cell carcinoma for gene therapy is possible.